This chapter focuses on adults with epilepsy and the nurse’s role in assisting patients to self-manage in the community setting and in caring for hospitalized patients with a seizure disorder. Although seizures and epilepsy are common in children, the special considerations related to children with these conditions are not addressed in this chapter. Other resources should be consulted for specific information on childhood and adolescent epilepsy.
People with epilepsy come into contact with nurses in many diverse settings along the health care continuum: schools, group homes, clinics, acute care hospital units, emergency departments (EDs), and intensive care units. The nurse-patient relationship will vary based on the care setting and the unique needs of the patient. Patients come in contact with the health care system in many ways. Whether providing education for self-management of their disorder or seizure first aid, sharing observations with the health care team to help diagnose the epilepsy, or providing direct patient care during seizures, there will be a caring nurse who will need to know about epilepsy and how it affects each patient. The focus of this chapter centers on care of the patient with epilepsy who is managed in the community by a primary care provider or a neurologist as well as care of the hospitalized patient with epilepsy. The patients and their family are at the center of this team as participators in their care. Epilepsy is often a lifelong disorder and education is required throughout the lifespan.
Primary care providers, neurologists, and nurse practitioners in the community manage many patients with epilepsy. Those with refractory epilepsy may be referred to an epilepsy center where an epileptologist and a multidisciplinary team provide comprehensive management, addressing the many issues and needs of these patients. Nurses and advanced practice nurses are key in providing direct care, promoting self-management, and educating patients and their families so that they can live the most healthy and productive lives possible.
ENTRY INTO HEALTHCARE
The ED can be the entry of care for patients with a first-time seizure, as well as for those with an established diagnosis of epilepsy. Close to 5% of the population of the United States will have at least one seizure that occurs without the presence of fever in their lifetime. Providers evaluate and treat patients acutely in the hopes of preventing further seizures or related complications. The emphasis is on identifying the underlying cause of the seizure, initiating treatment, and determining the need for additional evaluation. Nurses who practice in a hospital are likely to care for a patient who has a seizure secondary to metabolic imbalances, vascular abnormalities, or infections; it is important for them to be able to identify the various types of seizures that may occur. These types of seizures are partial or generalized in onset. Providing descriptive information about witnessed seizures will assist the team in diagnosing and treating the disorder.
BACKGROUND AND DEFINITIONS
Epilepsy was one of the first disorders described that involved the brain. The Babylonians described strange behaviors underwritten to superstition and witchcraft. The Greek defined epilepsy as a violent spasm. Some thought that demons and gods granted special visits to patients with such attacks. However, in 400 bc, the father of medicine, Hippocrates, stated that the strange disorder originated in the mind without clear understanding of how it originated or occurred. Ill-defined explanations about seizures continued until the 1870s when Jackson theorized that seizures originated from a localized, discharging focus in the brain. The introduction of the electroencephalogram (EEG) by Berger in 1929 provided the first recordings of epileptic discharges. This landmark event was followed in the 1930s by the work of Gibbs, who correlated the clinical indicators of epilepsy with EEG patterns. The development of classification systems for both epilepsies and seizures has paved the way to a better understanding of the variations in clinical presentation. Research focused on the clinical and cellular bases for seizures, new drugs, and improved management protocols have all contributed to better outcomes for patients subject to seizures.
The terminology for seizures and epilepsy is imprecise. The following widely accepted definitions have helped overcome imprecise terminology, which have created confusion about seizures and epilepsy in the past. This glossary summarizes the magnitude of definitions provided by the International League of Epilepsy.1 It is intended to provide a standard terminology for ease in communicating what is observed or reported by the presentation of the event that occurs. The terminology provided includes some definitions and comprehensive descriptions, along with supported etiology and pathophysiology. http://www.icnapedia.org/content/wiki/index.php/ILAE_Classification_and_Terminology_of_Seizures_and_Epilepsies (retrieved January 2012).
Aura: a premonitory sensation or warning experienced at the beginning of a seizure, which the patient remembers. An aura may be a gustatory, visual, auditory, or visceral experience such as a metallic taste or flashing lights. If a patient has an aura, it usually is the same experience each time.
Automatisms: defined as more or less coordinated, involuntary motor activities that occur during a state of impaired consciousness either in the course of or after an epileptic seizure, for which the person is usually amnesic. Several different types of automatism have been recognized. Examples of oral automatisms are lip smacking and chewing; manual automatisms can include picking at one’s clothing, fidgeting, or pacing.2 Automatisms are often associated with temporal lobe seizures, but can also occur with complex partial seizures, absence seizures, as well as other types of seizures.
Autonomic symptoms: can occur as a result of stimulation of the autonomic nervous system (e.g., epigastric sensation, pallor, sweating, flushing, piloerection, pupillary dilation).
Catamenial: refers to menses or menstruation; the term is used to describe a characteristic of a woman with epilepsy who has a tendency for seizures to occur at various times throughout the menstrual cycle.
Clonus: a term used to describe spasms in which a continuous pattern of rigidity and relaxation is repeated. In the second phase of a generalized seizure, called the clonic phase, rhythmic movements are followed by muscle relaxation. In the clonic phase, the rhythmic repeat movements again and again.
Cortical dysplasia: an abnormality in the development and organization of the cerebral cortex that can cause seizures and other neurological disorders. These disorders can result from abnormal migration of nerve cells during neural tube development in utero or can occur with some disorders of epilepsy.
EEG is a vital diagnostic procedure because it identifies patterns of abnormal electrical activity that can be correlated with particular types of seizure patterns. An EEG can also aid in lateralization and localization of an epileptogenic trigger focus.
Epilepsy: defined as more than one unprovoked seizure. It is a chronic disorder of abnormal, recurrent, excessive, and selfterminating discharges from neurons. Periods between seizures can vary widely and can be measured in minutes, hours, days, weeks, months, or even years. However, there is repetition of seizure activity at some time in the future, regardless of the time interval. Clinically, epilepsy is characterized by recurring seizures accompanied by a disturbance in some type of behavior (i.e., motor, sensory, autonomic, consciousness, or mentation). Epilepsy can be classified as idiopathic, cryptogenic, symptomatic, generalized, focal, or partial. Idiopathic means without a cause; cryptogenic means there is a likely cause, but it has not been identified; symptomatic means that a cause has been identified; generalized means that the seizures are involving the whole brain at once; and focal or partial means that the seizure starts from one area of the brain.
Epilepsia partialis continua: a continuous or prolonged partial seizure that causes contraction of the muscles. It is usually restricted to the muscles of the face, arm, or leg; it is usually not associated with impairment of consciousness.
Epileptic syndrome: an epileptic disorder characterized by a cluster of signs and symptoms customarily occurring together.
Epileptogenesis: sequence of events that converts a normal neuronal network into a hyperexcitable network. The concept of this is important for nurses to understand mechanism of action for medications.
Ictus: refers to an actual seizure; a seizure may be referred to as an ictal event.
Idiopathic generalized epilepsies: epilepsy syndromes characterized by discharges at onset from both hemispheres of the brain simultaneously, often genetic.
Intractable: difficult to alleviate, remedy, for example, intractable seizures are difficult to control with the usual antiepileptic drug (AED) therapy.
Jacksonian march: the spread of abnormal electrical activity from one area of the cerebral cortex to adjacent areas.
Nonconvulsive status epilepticus: used to denote a range of conditions in which electrographic seizure activity is prolonged and results in nonconvulsive clinical symptoms; even within a specific condition (e.g., complex partial and absence status epilepticus). The treatment and prognosis depend on the context in which the condition occurs.
Postictal: refers to the period immediately after a seizure has occurred.
Prodromal: refers to symptoms, such as a headache or feeling of depression which precede a seizure by hours.
Reflex epilepsy: a condition in which seizures can be provoked habitually by an external stimulus or, less commonly, internal mental processes.
Seizure: a single (finite) event of abnormal discharges in the brain which results in an abrupt and temporary altered state of cerebral function. Anyone can have a seizure under the right conditions.
Seizure disorder: a term adopted by some clinicians when referring to epilepsy. Although use of this term has led to some confusion, the terms epilepsy and seizure disorder are used interchangeably.
Semiology: the branch of linguistics concerned with signs and symptoms present during the ictal state.
Status epilepticus: more than 5 minutes of continuous seizure activity or two or more sequential seizures without full recovery of consciousness between seizures.3
Tonus: the degree of tone or contraction present in muscle when it is not undergoing shortening such as when muscle contracts and shortens.
Todd’s paralysis: a temporary, focal weakness or paralysis following a partial or generalized seizure that can last for up to 24 hours. The deficit can be correlated with an epileptic focus on the motor strip. Temporary neuronal exhaustion is probably the physiologic basis for the deficit.
SUDEP: defined as sudden, unexpected, nontraumatic, nondrowning death in an individual with epilepsy, witnessed or unwitnessed, in which postmortem examination does not reveal an anatomical or toxicological cause for the death.
Video EEG monitoring: a technique for recording the behavior and the EEG of a patient simultaneously. Changes in behavior can be correlated with changes in the EEG; useful for making the diagnosis of epilepsy and localizing the seizure focus.
A detailed list of additional definitions and terms are available on the ILAE website, http://www.icnapedia.org/content/wiki/index.php/ILAE_Classification_and_Terminology_of_Seizures_and_Epilepsies (retrieved January 2012).
Epidemiology and Risk Factors
Epilepsy is one of the most common neurological conditions representing a heterogeneous collection of disorders that have in common a recurrence of seizures. Three million people in the United States have epilepsy and 3,00,000 have their first event each year; 1,20,000 are children under the age of 18 years. Ten percent of Americans will have a seizure within their lifetime. Each year 2,00,000 new cases of epilepsy are diagnosed; for 70% of those diagnosed, there is no known cause.4 Approximately 30% of all epilepsies and 60% of all childhood epilepsies may have a significant genetic susceptibility. The risk of epilepsy is about 1% from birth through 20 years and 3% for the 70-year and older age group. The prevalence and cumulative incidence of epilepsy and partial seizures increase in the elderly.1
It is important to understand that anyone can have a seizure, given the right circumstances of central nervous system (CNS) imbalance, and each person has a unique threshold at which they will have a seizure if provoked. Repetitive, unprovoked seizures or epilepsy can develop secondary to an underlying etiology such as a traumatic brain injury, CNS infection, or brain tumor. For those with epilepsy, seizures may occur in patterns related to triggers that can lower the seizure threshold. If possible, it is important for patients to identify any seizure triggers so that they can be avoided. The major risk factors for developing seizures can be classified according to age group. In young adults, trauma, alcohol withdrawal, illicit drug use, brain tumor, and other CNS conditions are the most common causes. In the 35-year and older age group, cerebrovascular disease, brain tumor, alcohol withdrawal, metabolic disorders (e.g., uremia, electrolyte imbalance), Alzheimer’s disease, neurodegenerative diseases, and idiopathic causes rank as the major causes of seizures. The term idiopathic epilepsy is used for the 70% of all cases for which no specific cause is identified.
Mortality
Patients with epilepsy have a higher mortality rate than the general population. Close to 45,000 people with epilepsy die each year. The mortality rate is 20% in those who experience seizures lasting longer than 30 minutes. Those with generalized tonic-clonic seizures and status epilepticus have a three- to fourfold higher chance of dying. Deaths from accidents such as drowning, burning, trauma or choking, status epilepticus, suicide, and sudden unexpected death in epilepsy (SUDEP) are responsible for 50% of deaths in persons with epilepsy. Accidental deaths are often preventable and adherence to medication regimens is important to provide seizure control.5 Drowning and death from a motor vehicle, closed head injuries, and burns are some of the most feared injuries that concern the patient with epilepsy.
Clinical Pearl: Nurses should review safety issues including taking showers instead of baths, swimming with a companion rather than alone, and the use of flotation devices with water activities to minimize the chance of accidental drowning. Patients with uncontrolled seizures should not operate vehicles, heavy machinery, climb heights, or partake in any activities that may cause harm to them or to others if there were to have a seizure.
The person with epilepsy struggles to maintain a sense of self-management as they experience life changes that contribute to their fears. They are often told that they cannot drive, have others live in fear because of what they are experiencing, and require medications that affect their mood and disposition.
The incidence of depression in persons with epilepsy is close to five times higher than that of the entire population, and those with epilepsy have higher rates of suicide. AEDs can also contribute to depression and patients should be evaluated for this throughout their lifetime. Treatment with selective serotonin reuptake inhibitors (SSRIs) is common; although they can lower a seizure threshold in some individuals, they are commonly used to treat depression in this population.
Clinical Pearls: Patients with epilepsy should be frequently screened for depression with treatment options made available to them. The nurse can support depression screening and educate the patient regarding treatment and self-management.
Recognition that morbidity and mortality rates are higher in those with uncontrolled seizures provides nurses with opportunities to present valuable information to patients and families in a variety of settings.
As defined in the glossary, SUDEP is a sudden, unexpected, nontraumatic, nondrowning death in an individual with epilepsy, witnessed or unwitnessed, in which postmortem examination does not reveal an anatomical or toxicological cause for the death. The incidence of SUDEP is 0.35 per 1,000 persons with controlled seizures and 9.3 per 1,000 for those with medically refractory epilepsy. It is more common in persons with primary generalized epilepsy, a structural lesion on MRI, uncontrolled generalized tonic-clonic seizures, polypharmacy, and developmental delay. This unexpected cause of mortality exceeds close to 20 times the death rates in individuals afflicted with epilepsy compared to the population as a whole. In SUDEP, death can be witnessed or unwitnessed; there is no evidence of trauma, drowning or status epilepticus, and a seizure may or may not be noted.6 These diagnostic findings are confirmed on autopsy. Although discussions with patients can be awkward, SUDEP should be reviewed, especially with those at highest risk. The importance of adhering to medication regimen should be stressed to minimize chances of SUDEP. Resective surgery and improved seizure control decrease the risk of SUDEP in those with refractory localization-related epilepsy; temporal lobe resection has been shown to significantly reduce the mortality by improving seizure control.2 Research is geared toward identification of the mechanism supporting the explanation of SUDEP occurrence. Cardiac and respiratory abnormalities have been identified postmortem. There is ongoing research into investigation about separating evidence of apnea with respiratory arrest and the correlates to the CNS.3
Statistics on SUDEP are difficult to come by given the infrequency and underreporting by medical examiners and the overall lack of awareness of potential causes. People with epilepsy, their families, and the professional health care team work together to advocate the importance of confirming the diagnosis and discussing the treatment options, including information and education on quality of life. Recommendations also include advocating that of all patients with epilepsy having discussions with their providers regarding the potential cause of death with SUDEP, this is especially true in patient populations at higher risk.
Pathophysiology
Seizures are transient episodes of abrupt and temporary alteration of cerebral function resulting from a paroxysmal high-frequency or synchronous low-frequency, high-voltage electrical discharge.5 Ropper and Brown note that seizures require three conditions: (1) a population of pathologically excitable neurons; (2) an increase in excitatory glutaminergic activity through recurrent connections to spread the discharge; and (3) a reduction in the activity of the normal inhibitory γ-aminobutyric acid (GABA) projection.6 Seizures result from an imbalance between excitation and inhibition within the CNS. Excessive excitation or excessive inhibition may occur in focal areas of the cerebral cortex (focal seizures) or over the entire cerebral cortex (generalized seizures). A focal or generalized increase in neuronal excitability may result from an energy failure of neurons producing transient depolarization or lack of local inhibition.
Epilepsy can also result from alterations in membrane potentials that predispose certain hyperactive and hypersensitive neurons to respond abnormally to changes in the cellular environment. The recurrent seizures appearing without warning resulting from uncharacteristic electrical firing defines the condition of epilepsy. A single seizure can occur in ideal conditions. The person experiencing epilepsy has changes in the brain that result in the abnormal firing of neurons. The aberrant electrical activity that underlies epilepsy is the result of biochemical processes at the cellular level promoting neuronal hyperexcitability and neuronal hypersynchrony. However, a single neuron, discharging abnormally, is insufficient to produce a clinical seizure, which occurs only in the context of large neuronal networks. Cortical and several key subcortical structures are involved in generating a seizure.
A brief review of the cellular basis for focal and generalized seizure activity, with specific attention to ion channels, the essential currency of neuronal excitability provides a basis for understanding seizure activity. The hypersensitive neurons have lowered thresholds for firing and can fire excessively, creating an epileptogenic focus from which the seizure emanates. The epileptogenic focus generates large numbers of autonomous paroxysmal discharges that can be enhanced or minimized, depending on the neurotransmitter that is active at the postsynaptic membrane. An epileptogenic focus can induce secondary epileptogenic foci in a synaptically related area and also in the opposite cerebral hemispheres through connecting pathways between the same anatomic areas. Understanding of pathological changes on the cellular basis for focal and generalized seizure types allows the nurse working with patients with epilepsy to pay special note to the ion channels that create the current required for neurons to obtain their excitability.
Precipitating Factors: Triggers
In some patients with epilepsy, seizures can be precipitated by various stimuli called triggers. Sometimes the trigger is very specific for a particular person. Common triggers include particular odors, flashing lights, and certain types of music. If a specific stimulus can be identified, then the pattern is called reflex epilepsy. Reflex epilepsy can be provoked by an external stimulus (flashing lights) or, occasionally, by an internal process set off in the brain, such as addition or subtraction. Reflex seizures are somewhat predictable in response to specific stimuli, and may coexist with spontaneously occurring seizures. They are epileptic, not psychogenic, and may occur as either focal onset or primary generalized seizures. A confirmatory diagnosis occurs in over 20% of persons with primary generalized epilepsy. Other general triggers include fatigue, sleep deprivation, hypoglycemia, emotional stress, febrile illness, alcohol consumption and certain drugs, constipation, menstruation, and hyperventilation. However, missed medications are the most common trigger that contributes to seizure activity. For the most part, once triggers have been identified, exposure can be limited. Controlling exposure to triggers is the usual treatment, along with standard antiepileptic medications.7
SEIZURE CLASSIFICATION AND OBSERVATIONS/IDENTIFICATION
Seizures and epilepsy have been classified for clinical and research purposes using several different forms. Most classification systems are complex and cumbersome to use. In 1981, the International League Against Epilepsy (ILAE) published a modified version of the International Classification of Epileptic Seizures that continues to be a useful classification system (Table 28-1).3
The following section briefly discusses partial and generalized seizures. Tonic-clonic seizures, as examples of generalized seizures, are described in greater detail because they are so common. Table 28-2 describes the major subtypes of partial and generalized seizures, and Table 28-3 classifies partial seizures by cerebral lobe involved.
TABLE 28-1 CLASSIFICATION OF SEIZURES
Partial (focal, local) seizures
Simple partial seizures (consciousness not impaired)
Focal motor (with and without jacksonian march)
Somatosensory or special sensory symptoms (e.g., simple hallucinations such as tingling, light flashing, buzzing)
With autonomic symptoms (e.g., epigastric sensation, pallor, flushing)
With psychic symptoms (disturbances of higher cerebral function)
Complex partial seizures (with impairment of consciousness)
Beginning as simple partial seizures and progressing to impairment of consciousness
With no other features
With features as in simple partial seizures
With automatism
With impairment of consciousness at onset
With no other features
With features as in simple partial seizures
With automatism
Partial seizures evolving to secondarily generalized seizures
Simple partial seizures evolving to generalized seizures
Complex partial seizures evolving to generalized seizures
Simple partial seizures evolving to complex partial seizures to generalized seizures
Generalized seizures (generalized bilateral without focal onset)
Absence seizures
Myoclonic seizures
Clonic seizures
Tonic seizures
Tonic-clonic seizures
Atonic seizures
Unclassified epileptic seizures (including all seizures that cannot be classified due to inadequate or incomplete data and some that defy classification)
From: Commission on Classification and Terminology of the International League Against Epilepsy. (1981). Proposal for revised clinical and electroencephalographic classification of epileptic seizures. Epilepsia, 22, 489-501.
Recent recommendations have been provided for updates of the classification system (Table 28-4). Recommendations attempt to simplify classification to improve understanding of seizure classification and focus on guidelines instead of complicated descriptive terms. Currently, these are only recommendations and gradual acceptance will be required for eventual changes in the classification system.8
Partial Seizures
Partial-onset seizures are also referred to as focal seizures and begin as electrical disturbance in defined, localized areas of the brain. This form of seizure includes over 50% of the partial-onset form of seizures. The complexity of the seizure makes it difficult to diagnose, and the seizures may go unrecognized. Complex partial seizures are more resistant to treatment than generalized seizures.9
There are three types of partial seizures: simple, complex, and complex seizures evolving into secondarily generalized seizures. Simple and complex seizures are distinguished on the basis of consciousness. In simple partial seizures, consciousness is not impaired; in complex partial seizures consciousness is impaired. The four subcategories of simple partial seizures are named for the areas of their presenting symptoms. These include motor, sensory, autonomic, and psychic seizures.
Seizures affecting the motor area can include rhythmic twitching of extremity or isolated muscle group; those affecting the sensory area can include sensory disturbance to an isolated part of the body. Those affecting the autonomic area can include unusual smell, and fear of panic. Visual and auditory hallucinations can occur.9
Complex partial seizures include both complex symptomatology and impaired consciousness. The patient can stare blankly into space, be mute or speak nonsensically, or have automatisms such as lip smacking, chewing, or picking at clothing. Partial seizures can evolve into secondarily generalized seizures. These seizures are further categorized based on the type of partial seizure that preceded the generalized seizure (i.e., simple partial seizure only, complex partial seizure only, or simple partial seizure evolving into complex partial seizure).7 Patients who experience secondarily generalized events often demonstrate a disturbing moan with convulsive movements in extremities.
Clinical Pearl: Partial seizures are often more difficult to control and are more likely to require polytherapy or trials of several medications.
Generalized Seizures
There are six categories of generalized seizures: absence, myoclonic, clonic, tonic, tonic-clonic, and atonic. Each seizure type has characteristic clinical and EEG findings that are outlined in Table 28-2. The absence seizure is subdivided into typical and atypical absence seizures according to the presence of different EEG patterns and clinical presentation. Clinically, atypical absence seizures have a less abrupt onset and termination and are of a longer duration. The most common type of generalized seizure is the tonic-clonic seizure, formerly called the grand mal seizure.
TABLE 28-2 MAJOR SUBTYPES OF PARTIAL AND GENERALIZED SEIZURES
TYPE
DESCRIPTION
EEG FINDINGS
Partial Seizures
Simple partial seizures
Motor
Symptoms depend on the motor region activated.
May remain focal or may spread to other areas on the motor strip, a process called “march”; seizures called jacksonian seizures. For example, the seizure may begin in the fingers of one side, and march to the hand, wrist, forearm, and arm on the same side of the body. The particular sequence of involvement is helpful in locating the epileptic foci on the motor strip in the hemisphere opposite the convulsive movement.
Focal motor attack may cause head to turn to side opposite epileptic foci.
Todd’s paralysis may result; lasts minutes to hours.
Continuous focal motor seizure is called epilepsia partialis continua.
Applies to all simple partial seizures: may show abnormal discharges in a very limited region; seizures originating from deep structures may not be noted with scalp electrodes.
Sensory
Arise from cortical sensory strip.
Usually feels like “pins and needles” or numbness; sometimes, spatial disorientation.
May march to other areas or may become a complex partial or generalized tonic-clonic seizure.
Special sensory symptoms may include visual seizures such as flashing lights or visual hallucinations, auditory seizures with various sounds, gustatory sensations such as metallic taste or primary tastes (salty, sweet, sour, or bitter), or vertigo and floating sensations.
Autonomic
May occur as simple partial seizures.
Psychic
Disturbance in a higher-level function (i.e., distortion of memory), distorted time, feeling of déjà vu, illusions, depersonalization, or hallucinations.
Usually occur with impairment of consciousness and become complex partial seizures.
Complex Partial Seizures
One category
Only symptoms may be impaired consciousness or it may progress to include automatisms; note automatisms may occur in partial or generalized seizures.
Simple partial seizure followed by impairment of consciousness resulting in a complex seizure with motor, sensory, autonomic, or psychic symptoms as described above.
All complex seizures: generalized 2-4 Hz spike waves
Partial Seizures Evolving to Secondarily Generalized Seizures
One category
Includes seizures that may evolve into generalized seizures: simple partial, complex partial, or simple partial evolving into complex and then to generalized seizures.
Generalized Seizures
Absence seizures
Note: may be seen along with tonic-clonic seizures
Typical absence seizures: common in children; characterized by brief interruption in consciousness without loss of postural control. Typically, there is an interruption of activity with a momentary lapse of consciousness lasting 3-30 secs. If talking, the speech stops or slows; if eating, the hand and mouth stop, and if patient is called, there is no response.
Typical absences: 3-Hz spike-wave complexes with abrupt starts and stops
During an attack, the eyes may appear vacant, stare, or roll upward; the eyelids may twitch.
Seizures occur a few times to hundreds of times per day; person may not be aware of them.
People who have several attacks daily most often experience difficulty in learning or employment because of inattention.
Atypical absence seizures—the lapse of consciousness is usually of longer duration and less abrupt in onset; more obvious motor signs.
Atypical absences: ≤2.5 Hz; slower spike-and-wave pattern, and more irregular
Myoclonic seizures
Sporadic jerks that are sudden, brief; contractions that are usually symmetric.
When confined to one area, it may be the face and trunk; one or more extremities; an individual muscle; or a muscle group.
Myoclonic jerks are rapidly repetitive or relatively isolated.
Common around time of sleep or awakening; must be differentiated from myoclonic jerks of nonepileptic myoclonus.
Bilateral, generalized epileptiform discharges, typically polyspikes
Clonic seizures
Repetitive, rhythmic clonic movements that are bilateral and symmetric.
Associated with symmetric spike-wave complexes
Tonic seizures
Stiffening of the musculature, mostly of the body, but may also involve the arms.
Low-voltage paroxysmal fast activity (10 Hz)
Atonic seizures
Abrupt loss of postural muscle tone; lasts 1-2 secs.
Consciousness is briefly impaired, but usually there is no postictal confusion.
This group includes all seizures that cannot be classified because of inadequate or incomplete data. This self-explanatory category is a catchall for seizures that do not conform to any of the other headings.
Description of Generalized Tonic-Clonic Seizures
A tonic-clonic seizure progresses through distinct phases including the prodromal, tonic, clonic, and postictal phases. The prodromal phase of irritability and tension may precede the seizure by several hours or days. Some individuals experience an aura, whereas in others the seizure begins without warning. Characteristically, the tonic-clonic seizure begins with a sudden loss of consciousness. Neuronal hyperexcitation spreads to the subcortex, thalamus, and upper brainstem, and consciousness is suddenly lost. In the tonic phase, there is a major tonic contraction (increased tonus) of the voluntary muscles so that the body stiffens with legs and arms extended. If standing, the person falls to the ground. The jaw tightens, teeth clench, and the tongue or inner cheek may be bitten as a result. A loud, low ictal cry is heard as tonic contraction of the diaphragm and intercostal muscles force air through the contracted larynx. The patient will appear dusky or cyanotic during this phase, as apnea occurs during this phase. Urinary incontinence is common, bowel incontinence is less common. In addition, the pupils dilate and are unresponsive to light. The tonic phase generally lasts less than 1 minute.
TABLE 28-3 SEIZURE ACTIVITY OF PARTIAL SEIZURES (SIMPLE, COMPLEX, AND SECONDARILY GENERALIZED) BY LOBE
CEREBRAL HEMISPHERE LOBE
DESCRIPTION
Frontal lobe epilepsy
Many overlapping syndromes with frequent brief attacks (<30 secs)
Simple-complex seizures
Focal motor seizures (from motor strip)
Supplemental area motor seizures
Tonic and postural signs and symptoms with preserved consciousness; frequent falls
Complex partial seizures
Complex motor activity, vocalization, and gestural automatism (may be sexual)
Common to proceed to secondarily generalized tonic-clonic seizures
Mesial temporal lobe epilepsy
Most common cause is hippocampal sclerosis
Mostly complex partial seizures with automatisms and psychic symptoms
Often preceded by an aura in 50-95% of patients; rising epigastric discomfort is the most common aura
Seizure may include
staring
oral or manual automatisms
olfactory and auditory illusions or hallucinations
unilateral dystonic posturing
Parietal lobe epilepsy
Usually simple, complex, and secondarily generalized seizures
>75% have somatosensory auras
May have a distorted body image, visual or auditory hallucinations
Usually proceeds to impaired consciousness and contralateral motor activity
Occipital lobe epilepsy
Most have visual auras
Elemental visual hallucinations (e.g., flashing lights, colored lights) or sometimes blindness, scotoma, or hemianopsia
Eye blinking, nystagmus, head deviation, tonic and clonic eye movement common
Visual phenomena usually contralateral to side of the seizure
Often progress to complex partial seizures or secondarily generalized seizure depending on pathways stimulated
TABLE 28-4 COMPARISON OF MAJOR CHANGES BETWEEN THE 1989 AND 1981 CLASSIFICATION AND TERMINOLOGY AND THE NEWLY PROPOSED TERMINOLOGY AND CONCEPTS (COMMISSION 1981, 1989)
OLD TERMINOLOGY AND CONCEPTS
RECOMMENDED NEW TERMINOLOGY AND CONCEPTS
Focal and Generalized
For seizures
Focal (previously “partial”): the first clinical and electroencephalographic changes indicate initial activation of a system of neurons limited to a part of one cerebral hemisphere.
Generalized: the first clinical changes indicate initial involvement of both hemispheres.
For epilepsies
Localization-related (focal, partial): epilepsies with focal seizures.
Generalized: epilepsies with generalized seizures.
Focal seizures are conceptualized as originating at some point within networks limited to one hemisphere.
Generalized seizures are conceptualized as originating at some point within and rapidly engaging bilaterally distributed networks.
These terms were abandoned as overarching categories for classifying epilepsies per se, as many syndromes include both seizure types; they may still apply in some but not all instances.
Etiology
Idiopathic: there is no underlying cause other than a possible hereditary predisposition.
Symptomatic: the epilepsy is the consequence of a known or suspected disorder of the central nervous system.
Cryptogenic: this refers to a disorder whose cause is hidden or occult. Cryptogenic epilepsies are presumed to be symptomatic.
Genetic: the epilepsy is, as best as understood, the direct result of a known or presumed genetic defect(s) in which seizures are the core symptom of the disorder. This attribution must be supported by specific forms of evidence.
Structural/metabolic: there is a distinct other structural or metabolic condition or disease that has been demonstrated to be associated with a substantially increased risk of developing epilepsy. These disorders may be of acquired or genetic origin. When of genetic origin, there is a separate disorder interposed between the gene defect and the epilepsy.
Unknown: the nature of the underlying cause is unknown; it may have a fundamental genetic basis (e.g., a previously unrecognized channelopathy) or it may be the consequence of an unrecognized structural or metabolic disorder not yet identified.
Focal Seizure Types
Complex partial: with impairment of consciousness.
Simple partial: consciousness not impaired.
Secondarily generalized (Note: this was not the terminology used in the 1981 document but has come into common use).
No specific classification is recommended. Seizures should be described accurately according to their semiologic features without trying to fit them into artificial categories.
Organizational Structure for Epilepsies
Hierarchically organized by localization-related, generalized, and undetermined. Within those groups, by etiology (idiopathic, symptomatic, cryptogenic).
No specific organization is proposed. Instead, a flexible approach depending on needs is advocated.
From: Berg, A. T., & Scheffer, I. E. (2011). New concepts in classification of epilepsies: Entering the 21st century. Epilepsia, 52(6), 1058-1062.
The clonic phase begins with a gradual transition from the tonicity of the tonic phase. Inhibitory neurons of the cortex, anterior thalamus, and basal ganglion nuclei become active, intermittently interrupting the tonic seizure discharge with clonic activity. The clonic phase is characterized by violent, rhythmic, muscular contractions accompanied by hyperventilation. The face is contorted, the eyes roll, and there is excessive salivation with frothing from the mouth. Profuse sweating and a tachycardia are common. Color returns to the face. There are times when the patient experiencing an event, has a cessation in breathing and temporality stops. Once the breathing resumes, color returns to the face.
In the postictal phase, the clonic jerking gradually subsides in frequency and amplitude over a period of about 30 seconds, although it may be longer. The involved cells cease firing. The extremities are limp, breathing can be quiet or loud due to airway obstruction, and the pupils, which may be equal or unequal, begin to respond to light. Upon awakening, most patients are confused, disoriented, and amnesic for the event. Headache, generalized muscle aching, and fatigue are common. If undisturbed, the patient often falls into a deep sleep for several hours. There may also be temporary paresis, aphasia, or hemianopia. Following a seizure (i.e., generalized or partial), focal weakness, called Todd’s paralysis, may occur and last up to 24 hours. If it occurs, the focal deficit is important in localization of a focal epileptogenic site.
Because the seizure frequently occurs without warning, it is possible for injury to be sustained from falls or other accidents related to the seizure. Head injury, fracture of the limbs or vertebral column, burns, and shoulder dislocations are examples of serious injuries that may occur as a result. Tonic-clonic seizures may occur at any time of the day or night, whether the patient is awake or asleep. The frequency of recurrence can vary from hours to weeks, months, or years.
Clinical Pearl: Tonic-clonic seizures are dramatic and can be frightening to witness. They are usually self-limited, lasting less than 1 to 3 minutes. It is important for the nurse to stay calm, to provide first aid to the patient and reassurance to onlookers.
Status Epilepticus
Although there are many definitions of status epilepticus, it is generally defined as continuous seizures lasting longer than 5 minutes or two or more seizures without complete recovery in between. The most common cause of status epilepticus is abrupt discontinuation of AEDs. Other causes include alcohol withdrawal, acute neurological illness, metabolic disorders, or stroke. There are some forms of status epilepticus that tend to occur in the ambulatory settings, which will be discussed briefly here. A more in-depth review of convulsive status epilepticus and treatment will be found later in the chapter.
Absence Status Epilepticus
Absence status epilepticus is a prolonged confusional state in which the patient can function to some degree and is associated with generalized discharges on EEG that can last from hours to days. It occurs in those with idiopathic generalized epilepsy and has been referred to as spike-wave stupor, petit mal status, and absence status. It is seen in the outpatient setting; it is not life threatening. Absence status epilepticus is treated with benzodiazepines given by the intravenous (IV) route in the ED. An EEG is useful to the diagnosis and response to treatment and maintenance of current AEDs to prevent further episodes.10, 11
Simple Partial Status Epilepticus
Patients with simple partial status epilepticus (SPSE) present with focal, uncontrolled motor movements or sensory distortions such as déjà vu, imaginary sights, smells, tastes, or imaginary sounds, depending on the location of the seizure focus. The individual has preserved awareness during the event, which can be treated with a benzodiazepine and routine AEDs.12
Complex Partial Status Epilepticus
Patients with complex partial status epilepticus have impairment of consciousness or appear to be in an altered state of awareness of their environment. They exhibit strange behavior, and the duration of the seizure can be long, sometimes lasting for days. The seizure focus is commonly the temporal lobe; history and EEG can confirm diagnosis. Treatment with a benzodiazepine will usually break the seizure, and maintenance with traditional AEDs is recommended.10
Clinical Pearl: These types of status epilepticus are seen in the ambulatory settings and usually respond well to treatment with oral or IV benzodiazepines. They are nonlife threatening, but can be frightening or upsetting to patients or family members.
Epileptic Versus Nonepileptic Events
Seizures may also be classified as either epileptic or nonepileptic in nature. Epileptic seizures include partial and generalized seizures discussed earlier. Nonepileptic seizures or nonepileptic events number close to 30% of referrals to epilepsy centers. The clinical presentation often resembles that of an epileptic seizure, yet they fail to respond to standard treatment with AEDs because they are not epileptic. Nonepileptic events can be physiologic (seizures due to syncope) or psychogenic nonepileptic seizures (PNES). Patients have often failed trials of multiple AEDs and other treatments used to treat epilepsy and this should be a clue that a misdiagnosis has been made and further studies are required to characterize events.
Psychogenic Nonepileptic Seizures (PNES)
It is noted that PNES are more common in females and in those women with a history of physical, sexual, or emotional abuse; they are present without any evidence of an underlying pathological condition. The current understanding of PNES is that it is a conversion disorder which occurs on a subconscious level where the primary gain for expression of repressed trauma is that of anxiety relief. Secondary gains may be present and can include time off from work, kindness, attention and concern from an abuser, and release of responsibilities. Some believe that PNES is a form of dissociation and is now being seen in veterans returning from war with posttraumatic stress disorder. Other comorbidities seen with PNES include depression, anxiety, PTSD, and other somatoform presentations. Those who have confirmed epilepsy can also experience PNES, which makes treatment challenging. The prognosis is worse the longer the problem continues without treatment; it takes on average 7 years to diagnose the disorder.13
The term pseudo seizure has been used in the past and should be discouraged because it implies that one is “faking” a seizure. It is not to be confused with malingering, which is feigning a mental or physical disorder in order to avoid something such as going into the military, or to achieve something such as compensation for involvement in a motor vehicle accident. Malingering is intentional and cases are rare.
The diagnosis of PNES begins with evaluating the history of seizures, past treatments, and risk factors for PNES. The ictal characteristics of PNES are different from those having epileptic seizures and can include asynchronous body movements with flapping of the extremities, pelvic thrusting, stuttering, screaming, weeping, and often the eyes are closed. Symptoms are often dramatic, can start slowly, and wax and wane over 30 minutes, whereas an epileptic seizure usually has sudden onset with a duration of 1 to 2 minutes.14, 15
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